Mesenchymal precursor cells maintain the differentiation and proliferation potentials of breast epithelial cells

Duss, Stephan; Brinkhaus, Heike; Britschgi, Adrian; Cabuy, Erik; Schaefer, Dirk J.; Bentires‐Alj, Mohamed

doi:10.1186/bcr3673

Cited by 20 publications

(16 citation statements)

References 64 publications

(92 reference statements)

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“…Indeed, many organoid and co-culture studies have reported variable requirements for mesenchyme signaling to support epithelial progenitor cells and differentiation ex vivo (Chou et al, 2016;Hegab et al, 2015;Wells et al, 2013). Of particular note, in some studies, soluble factors can substitute for mesenchyme to promote some epithelial characteristics (Rebustini and Hoffman, 2009;Sequeira et al, 2010;Steinberg et al, 2005) and other studies demonstrate a requirement for direct contact of the mesenchyme to support epithelial differentiation (Duss et al, 2014;Lee et al, 2014;Li et al, 2004;Park et al, 2014). FGF signaling is required for development of salivary glands and other branched organs (Hoffman et al, 2002;Lombaert et al, 2013;Miralles et al, 1999;Patel et al, 2006;Steinberg et al, 2005;Zhang et al, 2014); however, the cell types that require FGF signaling are incompletely understood.…”

Section: Discussionmentioning

confidence: 99%

FGF2-dependent mesenchyme and laminin-111 are niche factors in salivary gland organoids

Hosseini

Nelson

Moskwa

et al. 2018

Journal of Cell Science

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Epithelial progenitor cells are dependent upon a complex 3D niche to promote their proliferation and differentiation during development, which can be recapitulated in organoids. The specific requirements of the niche remain unclear for many cell types, including the proacinar cells that give rise to secretory acinar epithelial cells that produce saliva. Here, using cultures of E16 primary mouse submandibular salivary gland epithelial cell clusters, we investigated the requirement for mesenchymal cells and other factors in producing salivary organoids in culture. Native E16 salivary mesenchyme, but not NIH3T3 cells or mesenchymal cell conditioned medium, supported robust protein expression of the progenitor marker Kit and the acinar/proacinar marker AQP5, with a requirement for FGF2 expression by the mesenchyme. Enriched salivary epithelial clusters that were grown in laminin-enriched basement membrane extract or laminin-111 together with exogenous FGF2, but not with EGF, underwent morphogenesis to form organoids that displayed robust expression of AQP5 in terminal buds. Knockdown of FGF2 in the mesenchyme or depletion of mesenchyme cells from the organoids significantly reduced AQP5 levels even in the presence of FGF2, suggesting a requirement for autocrine FGF2 signaling in the mesenchyme cells for AQP5 expression. We conclude that basement membrane proteins and mesenchyme cells function as niche factors in salivary organoids.

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Section: Discussionmentioning

confidence: 99%

FGF2-dependent mesenchyme and laminin-111 are niche factors in salivary gland organoids

Hosseini

Nelson

Moskwa

et al. 2018

Journal of Cell Science

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“…Overexpression of INHBA in mesenchymal cells increases colony formation potential of breast epithelial cells. 24 PTN, a secretory cytokine, has been found to stimulate breast cancer progression through remodeling of the tumor microenvironment. 25 Downregulation of SIAH2 has been found to be associated with resistance to endocrine therapy in breast cancer.…”

Section: Resultsmentioning

confidence: 99%

Assessment of Subnetwork Detection Methods for Breast Cancer

Jiang

Gribskov

2014

Cancer Inform

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Subnetwork detection is often used with differential expression analysis to identify modules or pathways associated with a disease or condition. Many computational methods are available for subnetwork analysis. Here, we compare the results of eight methods: simulated annealing–based jActiveModules, greedy search–based jActiveModules, DEGAS, BioNet, NetBox, ClustEx, OptDis, and NetWalker. These methods represent distinctly different computational strategies and are among the most widely used. Each of these methods was used to analyze gene expression data consisting of paired tumor and normal samples from 50 breast cancer patients. While the number of genes/proteins and protein interactions detected by the eight methods vary widely, a core set of 60 genes and 50 interactions was found to be shared by the subnetworks identified by five or more of the methods. Within the core set, 12 genes were found to be known breast cancer genes.

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“…It is unregulated in various tumors, such as lung cancer, breast cancer, meningeal glioma and so on [34][35][36] .…”

Section: Discussionmentioning

confidence: 99%

EIF4A3-Mediated CircRNA_100290 Promotes GC Cell Proliferation, Invasion and EMT via miR-29b-3p/ITGA11 Axis

Wang¹,

Sun²,

Li³

et al. 2020

Preprint

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Background Circular RNA (circRNA) has been reported as an important regulator in the development and progression of various carcinomas. However, the role of circRNA_100290 in gastric cancer (GC) is still unclear. This study aimed to investigate the role of circRNA_100290 in GC invasion and metastasis and its possible mechanism.Methods The expression of circRNA_100290 in GC cells and tissues were examined using quantitative real-time polymerase chain reaction (qRT-PCR). The role of circRNA_100290 in cell proliferation, migration, and invasion was evaluated on AGS and HGC-27 cell lines in vitro. Bioinformatics tools, dual-luciferase reporter assay, Western blot assay and qRT-PCR were used to explore the downstream pathways of circRNA_100290. The mechanism underlying the regulation of the expression of circRNA_100290 was explored using RNA immunoprecipitation, qRT-PCR, and Western blot assays.Results The expression of circRNA_100290 was found significantly upregulated in GC cells and 102 GC tissues, high expression of circRNA_100290 in GC was closely related to Borrmann’s types, lymph node metastasis and tumor-node-metastasis staging. In vitro, knockdown of circRNA_100290 in AGS and HGC-27 cells significantly inhibited cell proliferation, migration, and invasion. Mechanistically, dual-luciferase reporter assay confirmed a direct binding between circRNA_100290 and miR-29b-3p, which targets ITGA11, an oncogene which is closely related to epithelial–mesenchymal transition (EMT). In addition, EIF4A3, one of RNA binding proteins (RBPs), could inhibit the formation of circRNA_100290 via enriching flanking sites of circRNA_100290. Low expression of EIF4A3 in GC was related to a worse prognosis.Conclusions Elevated circRNA_100290 in GC promotes cell proliferation, invasion and EMT via miR-29b-3p/ITGA11 axi and might be regulated by EIF4A3. CircRNA_100290 might be a promising biomarker and target for GC therapy.

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Mesenchymal precursor cells maintain the differentiation and proliferation potentials of breast epithelial cells

Cited by 20 publications

References 64 publications

FGF2-dependent mesenchyme and laminin-111 are niche factors in salivary gland organoids

FGF2-dependent mesenchyme and laminin-111 are niche factors in salivary gland organoids

Assessment of Subnetwork Detection Methods for Breast Cancer

EIF4A3-Mediated CircRNA_100290 Promotes GC Cell Proliferation, Invasion and EMT via miR-29b-3p/ITGA11 Axis

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